通过调节Keap1/Nrf2/HO-1通路,SeMet可以缓解LPS诱导的卵腺死介导炎症
Dan Chen1, Wenying Sun1, Huanyi Liu1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.
Archives of biochemistry and biophysics
|December 5, 2023
概括
有机 (氨酸) 通过调节Keap1/Nrf2/HO-1通路,在蛋腺组织中减轻氧化应激和亡,保护产母免受脂多糖诱导的炎症.
科学领域:
- 动物科学动物科学
- 营养生物化学 营养生物化学
- 兽医病理学 兽医病理学
背景情况:
- 脂聚糖 (LPS) 暴露会导致各种组织的炎症.
- (Se) 对于减轻炎症损伤至关重要,有机形式如甲 (SeMet) 提供更好的吸收和更低的毒性.
- 蛋腺容易受到LPS引起的损伤,影响着产母的生产力.
研究的目的:
- 调查SeMet对LPS引起的对Hy-Line Brown产母蛋腺组织的保护作用.
- 阐明潜在的分子机制,包括氧化应激,亡和炎症途径.
主要方法:
- 棕色的Hy-Line产卵被分配到对照组,LPS,SeMet和SeMet + LPS组.
- 组织病理学检查 (H&E染色,TEM) 评估了组织损伤.
- 测量了氧化应激标志物 (MDA,SOD,CAT,GPX,GSH) 的含量.
- 使用qRT-PCR和西式涂抹,评估了Keap1/Nrf2/HO-1通路,亡 (RIPK1,RIPK3,MLKL) 和炎症 (TNF-α,COX-2,NF-κB) 的mRNA和蛋白质水平.
主要成果:
- 随着LPS的挑战,恶性甲酸 (MDA) 和炎症标志物 (Keap1,RIPK1,RIPK3,MLKL,TNF-α,COX-2,NF-κB) 增加,同时降低了抗氧化酶活动 (SOD,CAT,GPX) 和谷氨 (GSH).
- 此外,LPS还降低了Nrf2通路组件 (Nrf2,HO-1,NQO1) 和亲细胞亡标志物Caspase-8的水平.
- 补充SeMet有效地逆转了这些LPS诱导的变化,恢复了抗氧化剂状态,并通过Keap1/Nrf2/HO-1通路抑制了亡和炎症.
结论:
- SeMet可以缓解产卵母LPS诱导的卵腺组织损伤.
- 保护机制包括调节Keap1/Nrf2/HO-1通路,从而减少死细胞灭绝中介的炎症和氧化应激.
- 通过减轻LPS诱导的炎症损伤,SeMet显示了改善产母健康和产量的潜力.
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